THE OTHER SIDE OF SLEEP: DISCOVERIES IN BRAIN PHYSIOLOGYDiscoveries in brain physiology—new understanding of the structure and functioning of the brain, information not available to Freud—also make it difficult for some scientists to accept his concepts of dreaming. One school of thought holds, for example, that the very processes at work in the sleeping brain are themselves directly responsible for dream activity. In this model the activity of rapid eye movement is believed to stimulate the neural pathways that connect the eyes to the brain. Such stimulation directly affects the motor regions of the brain, in turn generating dream images of movement; it can also affect the forebrain, thus triggering memories or causing feelings of emotion to enter the dream picture. This theory, however, fails to account for the fact that dreaming occurs, to one extent or another, in all stages of sleep—a fact I’ll expand on shortly.During REM sleep the brain experiences a firestorm of electrical activity, which some scientists refer to as the “dream state generator.” Originating in the pons (“bridge”), a structure that spans the gap between the midbrain and the medulla, this electrical activity spreads over the cerebral cortex, the structure responsible for thought and motor activity. The bizarre and random nature of dreams reflects the randomness of the electrical discharge. Obviously, the theories of Freud can be dispensed with in a scientific model that portrays dreams merely as arbitrary accumulations of images, like a scrambled television signal. Some investigators, however, carry the “dream generator” concept a step further. According to this school of thought, the creation of visual and auditory hallucinations may indeed be a random process. The actual dream, however, is the process by which the cortex tries to weave unconnected images, sounds, and feelings into some kind of meaningful fabric. Our unconscious wishes, then, may serve as the loom on which this fabric is woven. Contrary to Freud’s view, these wishes do not actually cause the dream, but they exploit the existence of confused signals by imposing their own order upon them.*287\226\8*
RA (RHEUMATOID ARTHRITIS) IN CHILDREN AND ADOLESCENTSChildren and adolescents can develop a form of RA known as juvenile rheumatoid arthritis or, more commonly, JRA. Despite the similarity in names, this is a condition that is entirely different from the adult form. The term JRA stands for more than one condition; in fact, we know of at least three different types of JRA: polyarticular onset JRA (meaning many joints are affected), pauciarticular JRA (meaning a few joints are affected), and systemic onset JRA (meaning systems beyond the joints are affected). The different types of JRA are very dissimilar from each other in terms of the joints involved and the symptoms that occur.Treatment of JRA is similar in some ways to the treatment of adult RA, but it is also different in many ways. For example, periodic eye examinations are required for some children with JRA because asymptomatic eye problems can develop. Many of the medications used to treat adult RA are also used to treat JRA, but doses differ, and the medications sometimes cause side effects in children which they don’t cause in adults. AH medications and side effects should be discussed with the pediatrician or the pediatric rheumatologist (a specialist whose training differs from that of the adult rheumatologist in many instances).Physical therapy and occupational therapy are even more important for children than for adults since, unlike adults, children are still growing. In addition, children’s joints are much more likely than adult joints to freeze up and lose range of motion.JRA affects children emotionally and socially differently than it affects adults, too, but the child’s parents are generally more emotionally upset by the arthritis than the child is. Often the parents overprotect the child, emotionally and physically, preventing the child from experiencing the carefree time that kids need. If you are the parent of a child with JRA, we recommend that you• avoid sheltering the child or preventing him or her from developing coping mechanisms that will be required long after you are no longer nearby to provide assistance.• not make the child feel that he or she is “sick.”• discuss the specifics of the child’s limitations with the rheumatologist before restricting the child’s activities.• consult a pediatric counselor who is experienced in chronic disease and who can guide you and the child through behavior problems.*126/209/5*
The incubation period is usually from one to four weeks but can be much longer.
The disease begins as single or multiple subcutaneous nodules usually on the genitalia, which erode through the skin to produce painless ulcers or exuberant granulations. Anorectal lesions may occur in homosexual mea
Secondary infection may contribute to necrotic debris on an ulcer and an offensive sanguineous or purulent discharge may result. Surrounding cellulitis rarely occurs. The lesions are soft and friable and easily torn during childbirth.
Fibrosis occurs but is not marked. Phimosis or lymphoedema of distal tissues is common in the active phase of the disease.
There may be spread by autoinoculation to more distant sites particularly on the head, neck, groins, thighs and abdomen. Systemic spread may lead to granulomatous lesions of the liver, spleen, bone or joints.
Buy generic pills – online pharmacy
Donovanosis is a mildly contagious, chronic progressively destructive infection caused by Calymmatobacterium granulomatis, a gram-negative, oval bacillus in which polar bodies are often prominent. The organism develops intracellularly and is difficult to culture. This disease occurs in tropical countries including Papua New Guinea and, although uncommon in Australia, appears to be endemic in Aboriginal people in northern and central parts of the country.
Donovanosis should be distinguished from other causes of genital ulceration including syphilis, chancroid, lymphogranuloma venereum, severe herpes, cutaneous amoebiasis and anogenital neoplasm by appropriate tests. The diagnosis is established by the demonstration of С granulomatis in smears from scrapings or biopsies from lesions. Smears can be made by pressing a clean glass slide on the cut surface of a biopsy. The organisms can be identified as bipolar rods in large mononuclear cells and are best seen in giemsa-stained smears.
Compare online pharmacy prices
The patient with early syphilis should return for repeat examination and serology at the following intervals:
at one month;
at regular 3 monthly intervals for 1 year, and
at 6 monthly intervals for the second year.
Patients with late syphilis should be followed indefinitely; patients with neurosyphilis should have periodic CSF examinations for at least 3 years.
The titre of the reagin test (VDRL or RPR) will fall until it becomes non-reactive or minimally reactive (e.g. 1/2) by the end of 2 years after effective treatment of early syphilis.
In late syphilis, low titres are usually found and only a slight reduction should be expected after treatment. In some cases, no change in titre occurs. Provided the CSF has been tested and found to be non-reactive, no further treatment is indicated.
This reaction is a consequence of treponemal destruction. It occurs 6 to 12 hours after commencing treatment and is a mild reaction with fever, headache, malaise, rigors and joint pain. The reaction lasts for several hours and does not recur. Symptoms are controlled by paracetamol and rest.
Only one course of treatment is normally necessary. Further treatment is indicated in the following circumstances:
where clinical symptoms or signs of syphilis persist or recur,
where initially high titres in the reagin test (e.g. VDRL 1/8 or greater or RPR 1/16 or greater) persist for a year or more after treatment; or
where there is a sustained four-fold increase in the titre of the reagin test (as may occur with reinfection in a successfully treated patient).
For any patient with syphilis who can not be treated with penicillin, specialist advice should be sought. A tetracycline such as doxycycline is the second line drag of choice. Erythromycin is less reliable and is rarely indicated. Recommended regimens for these drugs are:
Doxycycline 300 mg daily orally in single or divided doses for 15 days; OR
Erythromycin (not estolate) 500 mg 4 times daily orally for 15 days. Late latent syphilis
Doxycycline 300 mg daily orally in single or divided doses for 30 days OR
Erythromycin (not estolate) 500 mg 4 times daily orally for 30 days.
For patients with neurosyphilis, penicillin allergy should be confirmed as the effectiveness of treatment with other drags is uncertain.
Antenatal screening and control of early infectious syphilis are essential for the control of congenital syphilis. Seropositive women must be evaluated and treated promptly. Regardless of the stage of pregnancy, patients who are not allergic to penicillin should be treated with penicillin according the regimens above. Pregnant patients with confirmed penicillin sensitivity should be referred for specialist care. If erythromycin is used, patient and infant must be closely followed for possible treatment failure.
Benzylpenicillin 30 to 60 mg mg/kg (for neonates) daily intramuscularly or intravenously in 2 divided doses for a minimum of 10 days; or Aqueous procaine penicillin G 50 mg/kg daily intramuscularly for a minimum of 10 days or Benzathine penicillin G 50,000 units/kg in a single dose ONLY IF CSF IS NORMAL. If there is CNS involvement, extended treatment with benzylpenicillin is recommended.
Only penicillin regimens are recommended for neonatal congenital syphilis. Tetracycline should not be used for children under the age of 8 years. Infants with congenital syphilis should be referred for specialist advice.